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Research profile · Peptide

Semax

Also known as ACTH(4-7)-Pro-Gly-Pro

Early human — evidence level 3 of 4: Early human evidenceExperimental — UK regulatory status: Experimental — not authorised for human use in the UK

Overview

A synthetic heptapeptide derived from a fragment of adrenocorticotropic hormone, studied chiefly in Russian stroke research.

Category
Peptide
Highest evidence level identified
Early human evidence
Last scientifically reviewed
20 August 2026
Last regulatory review
20 August 2026

Mechanism under investigation

Semax is a synthetic heptapeptide combining the ACTH(4–7) fragment with a C-terminal tripeptide that confers resistance to enzymatic degradation. It is a melanocortin derivative lacking the corticotropic activity of the parent sequence. Proposed mechanisms centre on modulation of neurotrophin signalling and broad transcriptional effects on inflammatory and neurotransmitter gene clusters. These pathway assignments derive chiefly from rodent transcriptomic work and remain proposed rather than established in humans.

Research areas

  • Neuroprotection models
  • Neurotrophin signalling

These are fields in which the compound has been investigated. Listing a field is not a statement that anything was demonstrated within it.

Current evidence

In-vitro evidence

Cells, tissues or biochemical systems outside a living organism.

Cell-culture work is comparatively limited and largely subordinate to the animal transcriptomic programme. Studies in mouse embryonic stem cells report effects on survival under serum deprivation with little effect on neuronal differentiation.

Animal evidence

Studies in living non-human animals.

This is the strongest and most methodologically transparent tier. A sustained RNA sequencing programme in a rat model of transient cerebral ischaemia reports attenuation of ischaemia-induced transcriptional disturbance across roughly two thousand differentially expressed genes, with corroborating protein-level work. Much of this is published in mainstream international journals and is the most independently assessable part of the literature.

Human observational evidence

Studies observing people without assigning an intervention.

Sparse. A 2018 study reported changes in a plasma neurotrophin marker in post-stroke rehabilitation patients, but human biomarker work is thin and largely embedded in the same clinical programme rather than conducted independently.

Clinical-trial evidence

Studies assigning an intervention to human participants.

Only four records across a 231-paper literature carry a clinical-trial publication type. Three are Russian-language, the studies are small, and they are variously described as open-label, non-randomised or using non-concurrent comparison groups. The 1997 acute-stroke study compared 30 treated patients against 80 receiving conventional therapy, which is not a randomised allocation. ClinicalTrials.gov returns no registered studies.

Study limitations

  • The clinical literature is small, old and largely untranslated: four indexed trials, three in Russian, concentrated in a single journal. Western readers cannot readily appraise the primary reports.
  • Designs are weak. Open-label and non-randomised comparisons predominate, and the principal stroke study used an unmatched control group several times larger than the treatment arm.
  • No trial registration exists anywhere, so pre-registered protocols and endpoints cannot be checked and selective outcome reporting cannot be excluded.
  • Roughly 43 per cent of indexed records involve the peptide’s originator, so the preclinical mechanism work and the clinical claims are not independent of one another.

UK regulatory context

Experimental — not authorised for human use in the UK

A compound appearing in research literature that holds no UK authorisation for human use in any indication.

Source: The Human Medicines Regulations 2012, regulation 46 — prohibition on sale or supply of an unauthorised medicinal product (opens legislation.gov.uk in a new tab) (legislation.gov.uk)

Regulatory classification is jurisdiction-specific. A compound authorised elsewhere is not thereby authorised in the UK, and a supplier’s description of a substance does not determine how it is classified in law. See safety and regulation for the framework and the authoritative sources.

Safety and interpretation

Published reports describe the compound as well tolerated, including in older patients, but these derive from small, mostly unblinded studies with short follow-up and no registry-grade adverse-event capture. No regulator outside Russia has assessed its safety, and no long-term human safety data exist. Reported registration as a medicine in Russia could not be verified against an official Russian regulator database and confers no UK status in any case.

References